4 research outputs found

    Multi-spatiotemporal heterogeneous legacy effects of climate on terrestrial vegetation dynamics in China

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    Investigating vegetation–climate interactions is critical for understanding behavioral patterns of terrestrial ecosystems and formulating food security strategies. However, the multi-spatiotemporal legacy effects of climate on terrestrial vegetation remain unclear. In this study, we examined the dynamic trends of vegetation distribution and climatic factors at multiple temporal and spatial scales. Moreover, using cross-wavelet transform, wavelet coherence transform, and partial correlation analysis, a paradigm framework was established to determine the multi-spatiotemporal legacy effect of climate on vegetation in China in 2000–2019, as well as the response of different vegetation types. The results indicate a significant greening trend in China, accompanied by a warming and wetting pattern over the past 20 years. The phase difference of the wavelet coherence transform in the time-frequency domain revealed remarkable legacy effects and regional variations, indicating a complicated relationship between vegetation and climate. Meanwhile, different vegetation types exhibited heterogeneous responses of legacy effect of precipitation and temperature on multi-spatiotemporal scales; moreover, the lag time in spring was shorter than that in summer and autumn. The average legacy effect on different vegetation types was approximately 1–2 months. Therefore, the heterogeneity of the legacy effects is a complicated process of dynamic variation, which can be summarized as the comprehensive characteristics of vegetation response to climate with regional discrepancy, ecosystem category, and multi-temporal scale. These findings advance our understanding regarding the preference of vegetation to hydrothermal conditions across biomes and ecosystems and provide a future framework for elucidating the dynamic response of vegetation to other more complex factors in this warmer world. Furthermore, our results emphasize that multi-spatiotemporal legacy effects should be incorporated into the vegetation–climate interaction model and the formulation of macro-environmental management policies.</p

    Visualization 1: Kilowatt-level fiber amplifier with spectral-broadening-free property, seeded by a random fiber laser

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    The change of beam profile recorded when the output power gradually increases from 350 W to 630 W Originally published in Optics Letters on 15 November 2015 (ol-40-22-5311

    Presentation_1_Fructose Induces Pulmonary Fibrotic Phenotype Through Promoting Epithelial-Mesenchymal Transition Mediated by ROS-Activated Latent TGF-β1.pdf

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    Fructose is a commonly used food additive and has many adverse effects on human health, but it is unclear whether fructose impacts pulmonary fibrosis. TGF-β1, a potent fibrotic inducer, is produced as latent complexes by various cells, including alveolar epithelial cells, macrophages, and fibroblasts, and must be activated by many factors such as reactive oxygen species (ROS). This study explored the impact of fructose on pulmonary fibrotic phenotype and epithelial-mesenchymal transition (EMT) using lung epithelial cells (A549 or BEAS-2B) and the underlying mechanisms. Fructose promoted the cell viability of lung epithelial cells, while N-Acetyl-l-cysteine (NAC) inhibited such. Co-treatment of fructose and latent TGF-β1 could induce the fibrosis phenotype and the epithelial-mesenchymal transition (EMT)-related protein expression, increasing lung epithelial cell migration and invasion. Mechanism analysis shows that fructose dose-dependently promoted the production of total and mitochondrial ROS in A549 cells, while NAC eliminated this promotion. Notably, post-administration with NAC or SB431542 (a potent TGF-β type I receptor inhibitor) inhibited fibrosis phenotype and EMT process of lung epithelial cells co-treated with fructose and latent TGF-β1. Finally, the fibrosis phenotype and EMT-related protein expression of lung epithelial cells were mediated by the ROS-activated latent TGF-β1/Smad3 signal. This study revealed that high fructose promoted the fibrotic phenotype of human lung epithelial cells by up-regulating oxidative stress, which enabled the latent form of TGF-β1 into activated TGF-β1, which provides help and reference for the diet adjustment of healthy people and patients with fibrosis.</p
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